It is estimated that as many as 70 million Americans experience chronic pain, and a worldwide study has concluded that between 10% and 55% of the population experiences chronic pain. In contrast to acute pain, which is associated with an inflammatory response in the early stages of healing, the International Association for the Study of Pain defines chronic pain as pain that persists past the normal time of healing or past the healing phase following an injury, as discussed in Bonica, J. J., “The Management of Pain,” Lea & Febiger, Philadelphia, 1953 and Merskey, et al., “Classification of Chronic Pain Syndromes and Definitions of Pain Terms,” Second Edition, 1994, which are incorporated herein by reference. Examples of chronic pain include lower back pain, migraine, fibromyalgia, complex regional pain syndrome, cancer pain, and spinal cord injury pain, to name a few.
The mechanisms responsible for chronic pain are largely unknown, and its treatments are often unsuccessful. The technique of nerve ablation is a destructive method of treating chronic pain by interrupting the transmission of neural signals that contribute to painful circuitry. The technique requires a physician to pass a probe percutaneously into the vicinity of nerve suspected of causing chronic pain, and deliver ablative energy through the probe to the nerve.
Physicians have expressed a need, which has thus far been unmet, for an embodiment and quantitative method to direct the ablative probe to the nerve that contributes to the painful circuitry, to interrogate the nerve for its role in chronic pain, to treat the nerve without removing the probe, to immediately confirm that the nerve has been lesioned and is no longer viable, and to confirm that the lesion has successfully disrupted the chronic pain circuitry. The challenge in enabling a solution is inherent to the pain type. Unlike acute pain, or nociceptive pain, chronic pain is governed by plastic changes in the spinal cord, brain, and the periphery. The neuroplastic changes responsible for chronic pain may include augmentation or modification of existing circuitry, aberrant neural circuitry and/or changes enabled by non-neural structures. The most predictive markers of chronic pain are brain derived, and include: (1) Brain chemistry; (2) Cognition; (3) Brain morphometry; (4) Spontaneous fluctuations of pain; and (5) Brain activity.
In “Towards a theory of chronic pain”, Progress in Neurobiology, Vol. 87, No. 2, February 2009, pages 81-97, A. Vania Apkarian, Marwan N. Baliki, and Paul Y. Geha, the authors used functional magnetic resonance imaging (fMRI) to discern brain regions that where active in persons with chronic back pain. Accordingly, they found neural activation patterns in regions of the brain (medial prefrontal cortex) that are atypical of ordinary pain. The authors suggest that the activity and site can be used to mark chronic back pain. Despite fMRI's abilities to discern markers of chronic pain in humans, the technology itself is poorly suited for the clinical setting. Functional magnetic imaging technologies are expensive, take up valuable room space, require a controlled operating environment (i.e., non-ferromagnetic tools) and are unable to provide timely acquisition and analysis of recorded data (poor temporal resolution).
As such, there is an unmet need for a system or apparatus for identifying or locating a source of or neural pathway associated with chronic pain, as well as for treating the chronic pain once its source has been identified. There is also a need for a practical and effective method for identifying or locating a source of chronic pain or a neural pathway associated with chronic pain, as well as for treating the chronic pain once its source has been identified.